1. Field of the Invention
The present invention relates to an implantable coronary perfusion monitoring device according to the preamble of the independent claim.
2. Description of the Prior Art
For ischemic patients, the normal compensatory mechanism in autoregulating blood flow is generally decreased by the underlying cardiovascular disease (arteriosclerosis). It is therefore even more important for ischemic patients to get optimized coronary perfusion. This perfusion is adversely affected by arteriosclerosis due to:
A) the time-shift of the peripherally reflected pressure ways, and
B) the decreased compliance of the aorta, as described below.
In short, the present invention is inter alia based upon the theory of the so-called “Windkessel effect” and peripherally reflected pressure waves, resulting in a measure calculated through the use of various sensors (e.g. impedance sensors) which very effectively can monitor the conditions which are crucial for a good coronary perfusion.
Vascular mechanical properties are carefully matched with cardiac position, heart rate and timing of contraction in a young healthy person (or animal) to minimize afterload and maximize coronary perfusion. The pressure curve in the first part of aorta is determined not only by cardiac and local vascular properties, but also by the properties of the more distal elastic arteries, which is referred to as the “Windkessel effect” and reflection of pressure waves in the periphery (mainly in bifurcations and high resistance vessels).
The elastic (large) arteries expand during systolic ejection of blood from the left ventricle and recoil in diastole. The physiologic meaning of this is to decrease the rise of pressure during ejection and thereby facilitate ejection (i.e. minimize afterload) and also to increase pressure during diastole improving coronary perfusion pressure at the time when the heart is relaxed and can be perfused. The time constant of recoil is in a healthy person perfectly matched.
With increasing age and stiffening of the arteries both the time constant and the volume of blood that can be “stored” during systole decrease.
The reflection of pressure waves has a similar physiologic effect. The pressure waves (5-10 m/s) travel much faster than blood flow (<1 m/s). This means that waves reflected in the periphery come back to the heart during each ongoing beat. The wave speed is affected by many factors including blood pressure and stiffness of the vessels. The reflection coefficient is determined by the matching of vascular impedances. In a healthy person bifurcations are almost perfectly matched to avoid reflection of forward travelling waves. The main source of reflection in healthy person therefore is peripheral resistance vessels (arteriole). The summed effect of the reflected pressure waves is to increase diastolic pressure and facilitate coronary perfusion as above, while maintaining a low afterload.
With increasing age and arteriosclerosis reflection coefficients in vascular bifurcations increase and since wave speed also increases this causes the reflected waves to arrive back in the aortic root earlier (during early systolic ejection), thereby increasing afterload (lowering stroke volume) and causing premature closure of the aortic valve, without contributing to coronary perfusion. This is illustrated by the curves in FIG. 1. In the Figure the evolution of the aortic pressure curve with age is seen. The aortic pressure is denoted at the y-axis, and time is denoted at the x-axis. The left curve represents the pressure curve of a younger individual, the middle curve represents a middle-aged individual and the right curve an older individual. As clearly visible from the curves the point of time (t1, t2, t3) for the maximum pressure during diastole is earlier the older patient is. Furthermore, the difference between the maximum pressure values is increasing with age, which is illustrated by the lines in the Figure.
The intricate pathophysiology discussed above is extremely important when understanding the effects of cardiovascular disease. Arteriosclerosis is a problem far more complicated than “vascular stenosis”. The above mentioned phenomena are not only related to arteriosclerosis, but also to hypertension per se since vascular stiffness is non-linear. Wave speed and stiffness increase with increasing pressure. This may be functional in exercise with increasing heart rate and a modest rise in blood pressure, since the matching then is maintained, but is usually an unwanted effect in hypertensive disease.
When contemplating the facts above it becomes clear that optimal cardiovascular matching is dependant on heart rate, timing of ejection, blood pressure and vascular properties. These factors are all changing in short-term (ischemia, stress) and long-term (arteriosclerosis, remodelling, disease progression) in cardiac patients. It makes sense to monitor this matching both aiming to optimize treatment and also possibly warn the patient or doctor.
In the following some patent documents are listed which are related to some of the aspects discussed above.
U.S. Pat. No. 4,821,735 relates to a method and apparatus for detecting myocardial ischemia that monitors the systemic vascular resistance and detects the presence of myocardial ischemia when the systemic vascular resistance increases by at least sixty percent over a base line value.
The detection involves monitoring the arterial pressure to get a blood pressure signal. The first time derivative of the blood pressure signal is calculated and the peak of the dP/dt signal is determined. The pressure value corresponding in time to this identified peak in dP/dt is identified. The systemic vascular resistance is determined as the quotient between the identified pressure value and the peak dP/dt value.
U.S. Pat. No. 6,315,735 discloses an in-vivo technique for determination of the compliance of the vascular system downstream of a ventricle or the systemic blood flow from the blood pressure. The calculations are based upon the so-called Windkessel model.
U.S. Pat. No. 5,211,177 discloses determination of vascular impedance based upon arterial blood pressure and the modified Windkessel model.
WO-2005/014084 discloses an IMD capable of identifying periods of coronary perfusion based upon different signals collected by the IMD, such as pressure signals, oximetry signals, etc. and then to deliver a therapeutic and/or diagnostic agent to a heart during diastolic coronary perfusion for more optimal use of the agent.
There is a need for improved indication and monitoring of the status of coronary perfusion both for diagnostic and therapeutic purposes.